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  1. Article: The rat endovascular perforation model of subarachnoid hemorrhage.

    Sehba, Fatima A

    Acta neurochirurgica. Supplement

    2015  Volume 120, Page(s) 321–324

    Abstract: The rat endovascular perforation model is considered the closest replica of human condition. Since its development, this model has been extensively used to study early brain injury after subarachnoid hemorrhage (SAH). However, like any other animal model, ...

    Abstract The rat endovascular perforation model is considered the closest replica of human condition. Since its development, this model has been extensively used to study early brain injury after subarachnoid hemorrhage (SAH). However, like any other animal model, it has advantages and limitations. The following is a brief review of the rat endovascular perforation SAH model. One section is dedicated to technical considerations that can be used to overcome the model limitations.
    MeSH term(s) Animals ; Cerebrovascular Circulation/physiology ; Disease Models, Animal ; Endovascular Procedures/methods ; Rats ; Subarachnoid Hemorrhage/physiopathology
    Language English
    Publishing date 2015
    Publishing country Austria
    Document type Journal Article ; Review
    ISSN 0065-1419
    ISSN 0065-1419
    DOI 10.1007/978-3-319-04981-6_55
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Rat endovascular perforation model.

    Sehba, Fatima A

    Translational stroke research

    2014  Volume 5, Issue 6, Page(s) 660–668

    Abstract: Experimental animal models of aneurysmal subarachnoid hemorrhage (SAH) have provided a wealth of information on the mechanisms of brain injury. The rat endovascular perforation (EVP) model replicates the early pathophysiology of SAH and hence is ... ...

    Abstract Experimental animal models of aneurysmal subarachnoid hemorrhage (SAH) have provided a wealth of information on the mechanisms of brain injury. The rat endovascular perforation (EVP) model replicates the early pathophysiology of SAH and hence is frequently used to study early brain injury following SAH. This paper presents a brief review of historical development of the EVP model and details the technique used to create SAH and considerations necessary to overcome technical challenges.
    MeSH term(s) Animals ; Carotid Artery, Internal/surgery ; Disease Models, Animal ; Endovascular Procedures ; Female ; Male ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Subarachnoid Hemorrhage/etiology ; Subarachnoid Hemorrhage/physiopathology
    Language English
    Publishing date 2014-09-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2541897-X
    ISSN 1868-601X ; 1868-4483
    ISSN (online) 1868-601X
    ISSN 1868-4483
    DOI 10.1007/s12975-014-0368-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Early events after aneurysmal subarachnoid hemorrhage.

    Sehba, Fatima A / Friedrich, Victor

    Acta neurochirurgica. Supplement

    2015  Volume 120, Page(s) 23–28

    Abstract: The first 72 h after aneurysmal subarachnoid hemorrhage (SAH) is a critical period for the patient. Most of the deaths in the SAH patient population occur during this time, and a number of key events activate and trigger mechanisms that not only ... ...

    Abstract The first 72 h after aneurysmal subarachnoid hemorrhage (SAH) is a critical period for the patient. Most of the deaths in the SAH patient population occur during this time, and a number of key events activate and trigger mechanisms that not only contribute to early brain injury but evolve over time and participate in the delayed complications. This review highlights the contribution of key events to the early brain injury and to overall outcome after SAH.
    MeSH term(s) Brain Chemistry/physiology ; Brain Ischemia/metabolism ; Brain Ischemia/pathology ; Brain Ischemia/physiopathology ; Disease Progression ; Humans ; Hyperemia/metabolism ; Hyperemia/pathology ; Hyperemia/physiopathology ; Intracranial Hypertension/metabolism ; Intracranial Hypertension/pathology ; Intracranial Hypertension/physiopathology ; Subarachnoid Hemorrhage/metabolism ; Subarachnoid Hemorrhage/pathology ; Subarachnoid Hemorrhage/physiopathology
    Language English
    Publishing date 2015
    Publishing country Austria
    Document type Journal Article ; Review
    ISSN 0065-1419
    ISSN 0065-1419
    DOI 10.1007/978-3-319-04981-6_4
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  4. Article: Aneurysmal subarachnoid hemorrhage models: do they need a fix?

    Sehba, Fatima A / Pluta, Ryszard M

    Stroke research and treatment

    2013  Volume 2013, Page(s) 615154

    Abstract: The discovery of tissue plasminogen activator to treat acute stroke is a success story of research on preventing brain injury following transient cerebral ischemia (TGI). That this discovery depended upon development of embolic animal model reiterates ... ...

    Abstract The discovery of tissue plasminogen activator to treat acute stroke is a success story of research on preventing brain injury following transient cerebral ischemia (TGI). That this discovery depended upon development of embolic animal model reiterates that proper stroke modeling is the key to develop new treatments. In contrast to TGI, despite extensive research, prevention or treatment of brain injury following aneurysmal subarachnoid hemorrhage (aSAH) has not been achieved. A lack of adequate aSAH disease model may have contributed to this failure. TGI is an important component of aSAH and shares mechanism of injury with it. We hypothesized that modifying aSAH model using experience acquired from TGI modeling may facilitate development of treatment for aSAH and its complications. This review focuses on similarities and dissimilarities between TGI and aSAH, discusses the existing TGI and aSAH animal models, and presents a modified aSAH model which effectively mimics the disease and has a potential of becoming a better resource for studying the brain injury mechanisms and developing a treatment.
    Language English
    Publishing date 2013-06-26
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2573724-7
    ISSN 2042-0056 ; 2090-8105
    ISSN (online) 2042-0056
    ISSN 2090-8105
    DOI 10.1155/2013/615154
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Cerebral microvasculature is an early target of subarachnoid hemorrhage.

    Sehba, Fatima A / Friedrich, Victor

    Acta neurochirurgica. Supplement

    2013  Volume 115, Page(s) 199–205

    Abstract: Most subarachnoid hemorrhage (SAH) patients exhibit clinical signs of cerebral ischemia at admission but no angiographic vasospasm. Consequently, the source of early cerebral ischemia is not understood. Parenchymal microvessels may contribute to early ... ...

    Abstract Most subarachnoid hemorrhage (SAH) patients exhibit clinical signs of cerebral ischemia at admission but no angiographic vasospasm. Consequently, the source of early cerebral ischemia is not understood. Parenchymal microvessels may contribute to early cerebral ischemia, but the low resolution of current imaging has prevented their analysis in SAH patients. Animal studies demonstrated that early after SAH structure and function of parenchymal vessels are compromised to the level that may very well contribute to early ischemia. We review these studies.
    MeSH term(s) Animals ; Cerebral Cortex/pathology ; Disease Models, Animal ; Encephalitis/etiology ; Encephalitis/pathology ; Humans ; Microvessels/physiopathology ; Microvessels/ultrastructure ; Nervous System Diseases/etiology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/metabolism ; Oxidative Stress/physiology ; Signal Transduction/physiology ; Subarachnoid Hemorrhage/complications ; Subarachnoid Hemorrhage/pathology
    Chemical Substances Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase (EC 1.14.13.39)
    Language English
    Publishing date 2013
    Publishing country Austria
    Document type Journal Article ; Review
    ISSN 0065-1419
    ISSN 0065-1419
    DOI 10.1007/978-3-7091-1192-5_37
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Sexual dimorphism in gene expression after aneurysmal subarachnoid hemorrhage.

    Friedrich, Victor / Bi, Weina / Sehba, Fatima A

    Neurological research

    2015  Volume 37, Issue 12, Page(s) 1054–1059

    Abstract: Background and purpose: Inflammation and compromise in structure and function of cerebral parenchymal microvasculature begins early after subarachnoid hemorrhage (SAH). We recently found greater inflammation and greater vascular compromise in male than ... ...

    Abstract Background and purpose: Inflammation and compromise in structure and function of cerebral parenchymal microvasculature begins early after subarachnoid hemorrhage (SAH). We recently found greater inflammation and greater vascular compromise in male than in female rats following SAH. In this study, we investigated whether this cross-sexual difference in pathology is reflected in expression levels of genes related to vascular inflammation and structural compromise.
    Method: Age-matched male and female rats underwent sham surgery or SAH by endovascular perforation. Early physiology (intracranial pressure (ICP), blood pressure (BP), heart rate, and cerebral blood flow) was monitored. Cerebral RNA was extracted at sacrifice 3 h after surgery and assayed for expression of thrombomodulin (Thbd), endothelial nitric oxide synthase (eNos;Nos3), intracellular adhesion molecule-1 (Icam1), vascular endothelial growth factor (Vegf), interleukin-1beta (Il1β) tumor necrosis factor-alpha (Tnf-α), and arginine vasopressin (Avp).
    Results: Increases in ICP and BP at SAH appeared slightly greater in males but the difference did not reach statistical difference, indicating that SAH intensity did not differ significantly between the sexes. Of the seven genes studied two; Tnf-α and Vegf, did not change after injury, while the remainder showed significant responses to SAH. Response of Nos3 and Thbd was markedly different between the sexes, with expression greater in males.
    Conclusion: This study finds that sexual dimorphism is present in the response of some but not all genes to SAH. Since products of genes exhibiting sexual dimorphism have anti-inflammatory activities, our results indicate that previously found sex-based differences in vascular pathology are paralleled by sexually dimorphic changes in gene expression following SAH.
    MeSH term(s) Animals ; Arginine Vasopressin/genetics ; Arginine Vasopressin/metabolism ; Blood Pressure/physiology ; Cerebrovascular Circulation ; Disease Models, Animal ; Female ; Gene Expression Regulation/physiology ; Heart Rate/physiology ; Intercellular Adhesion Molecule-1/genetics ; Intercellular Adhesion Molecule-1/metabolism ; Interleukin-1beta/genetics ; Interleukin-1beta/metabolism ; Intracranial Pressure ; Male ; Phosphopyruvate Hydratase/genetics ; Phosphopyruvate Hydratase/metabolism ; Rats ; Rats, Sprague-Dawley ; Sex Characteristics ; Subarachnoid Hemorrhage/genetics ; Subarachnoid Hemorrhage/metabolism ; Subarachnoid Hemorrhage/physiopathology ; Thrombomodulin/genetics ; Thrombomodulin/metabolism ; Time Factors ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism
    Chemical Substances Interleukin-1beta ; Thrombomodulin ; Tumor Necrosis Factor-alpha ; Vascular Endothelial Growth Factor A ; Arginine Vasopressin (113-79-1) ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Phosphopyruvate Hydratase (EC 4.2.1.11)
    Language English
    Publishing date 2015
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 424428-x
    ISSN 1743-1328 ; 0161-6412
    ISSN (online) 1743-1328
    ISSN 0161-6412
    DOI 10.1080/01616412.2015.1115211
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  7. Article: Brain injury after transient global cerebral ischemia and subarachnoid hemorrhage.

    Sehba, Fatima A / Pluta, Ryszard M / Macdonald, R Loch

    Stroke research and treatment

    2013  Volume 2013, Page(s) 827154

    Language English
    Publishing date 2013-11-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2573724-7
    ISSN 2042-0056 ; 2090-8105
    ISSN (online) 2042-0056
    ISSN 2090-8105
    DOI 10.1155/2013/827154
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  8. Article: Early micro vascular changes after subarachnoid hemorrhage.

    Sehba, Fatima A / Friedrich, Victor

    Acta neurochirurgica. Supplement

    2011  Volume 110, Issue Pt 1, Page(s) 49–55

    Abstract: During the last decade much effort has been invested in understanding the events that occur early after SAH. It is now widely accepted that these early events not only participate in the early ischemic injury but also set the stage for the pathogenesis ... ...

    Abstract During the last decade much effort has been invested in understanding the events that occur early after SAH. It is now widely accepted that these early events not only participate in the early ischemic injury but also set the stage for the pathogenesis of delayed vasospasm. That early cerebral ischemia occurs after SAH is documented in both experimental SAH and in human autopsy studies; however, angiographic evidence for vasoconstriction early after SAH is lacking and the source of early ischemic injury is therefore unclear. Recently, the cerebral microvasculature has been identified as an early target of SAH. Changes in the anatomical structure of cerebral microvessels, sufficient to cause functional deficits, are found early after experimental SAH. These changes may explain cerebral ischemia in human in the absence of angiographic evidence of large vessel vasoconstriction. This paper summarizes known alterations in cerebral microvasculature during the first 48 h after SAH.
    MeSH term(s) Animals ; Basement Membrane/physiopathology ; Blood Platelets/metabolism ; Blood Vessels/physiopathology ; Endothelium/physiopathology ; Humans ; Subarachnoid Hemorrhage/complications ; Vasospasm, Intracranial/etiology ; Vasospasm, Intracranial/pathology
    Language English
    Publishing date 2011
    Publishing country Austria
    Document type Journal Article ; Review
    ISSN 0065-1419
    ISSN 0065-1419
    DOI 10.1007/978-3-7091-0353-1_9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Nitric oxide in early brain injury after subarachnoid hemorrhage.

    Sehba, Fatima A / Bederson, Joshua B

    Acta neurochirurgica. Supplement

    2011  Volume 110, Issue Pt 1, Page(s) 99–103

    Abstract: Nitric Oxide (NO) is the major regulator of cerebral blood flow. In addition, it inhibits platelet adherence and aggregation, reduces adherence of leukocytes to the endothelium, and suppresses vessel injury. NO is produced on demand by nitric oxide ... ...

    Abstract Nitric Oxide (NO) is the major regulator of cerebral blood flow. In addition, it inhibits platelet adherence and aggregation, reduces adherence of leukocytes to the endothelium, and suppresses vessel injury. NO is produced on demand by nitric oxide synthase and has a very short half life. Hence maintenance of its cerebral level is crucial for normal vascular physiology. Time dependent alterations in cerebral NO level and the enzymes responsible for its synthesis are found after subarachnoid hemorrhage (SAH). Cerebral NO level decreases, recovers and increases within the first 24 h after SAH. Each change in cerebral NO level elicits a different pathological response form already compromised brain. These response range from constriction, platelet aggregation and vascular injury that occurs during the early hours and delayed occurring vasospasm, neuronal and axonal damage. This review summarizes the underlying mechanism and the consequence of alteration in cerebral NO level on brain during the first 72 h after SAH.
    MeSH term(s) Animals ; Brain/metabolism ; Brain Injuries/etiology ; Brain Injuries/metabolism ; Brain Injuries/pathology ; Humans ; Nitric Oxide/metabolism ; Subarachnoid Hemorrhage/complications ; Time Factors
    Chemical Substances Nitric Oxide (31C4KY9ESH)
    Language English
    Publishing date 2011
    Publishing country Austria
    Document type Journal Article ; Review
    ISSN 0065-1419
    ISSN 0065-1419
    DOI 10.1007/978-3-7091-0353-1_18
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Gender influences the initial impact of subarachnoid hemorrhage: an experimental investigation.

    Friedrich, Victor / Bederson, Joshua B / Sehba, Fatima A

    PloS one

    2013  Volume 8, Issue 11, Page(s) e80101

    Abstract: Aneurysmal subarachnoid hemorrhage (SAH) carries high early patient mortality. More women than men suffer from SAH and the average age of female SAH survivors is greater than that of male survivors; however, the overall mortality and neurological ... ...

    Abstract Aneurysmal subarachnoid hemorrhage (SAH) carries high early patient mortality. More women than men suffer from SAH and the average age of female SAH survivors is greater than that of male survivors; however, the overall mortality and neurological outcomes are not better in males despite their younger age. This pattern suggests the possibility of gender differences in the severity of initial impact and/or in subsequent pathophysiology. We explored gender differences in survival and pathophysiology following subarachnoid hemorrhage induced in age-matched male and female rats by endovascular puncture. Intracranial pressure (ICP), cerebral blood flow (CBF), blood pressure (BP) and cerebral perfusion pressure (CPP) were recorded at and after induction of SAH. Animals were sacrificed 3 hours after lesion and studied for subarachnoid hematoma size, vascular pathology (collagen and endothelium immunostaining), inflammation (platelet and neutrophil immunostaining), and cell death (TUNEL assay). In a second cohort, 24-hour survival was determined. Subarachnoid hematoma, post-hemorrhage ICP peak, BP elevation, reduction in CPP, intraluminal platelet aggregation and neutrophil accumulation, loss of vascular collagen, and neuronal and non-neuronal cell death were greater in male than in female rats. Hematoma size did not correlate with the number of apoptotic cells, platelet aggregates or neutrophil. The ICP peak correlated with hematoma size and with number of apoptotic cells but not with platelet aggregates and neutrophil number. This suggests that the intensity of ICP rise at SAH influences the severity of apoptosis but not of inflammation. Mortality was markedly greater in males than females. Our data demonstrate that in rats gender influences the initial impact of SAH causing greater bleed and early injury in males as compared to females.
    MeSH term(s) Animals ; Apoptosis ; Blood Platelets/pathology ; Blood Pressure ; Brain/blood supply ; Brain/physiopathology ; Female ; Humans ; Inflammation/physiopathology ; Intracranial Pressure ; Male ; Neurons/pathology ; Neutrophils/pathology ; Rats ; Regional Blood Flow ; Sex Characteristics ; Subarachnoid Hemorrhage/physiopathology
    Language English
    Publishing date 2013-11-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0080101
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